Objective To investigate the mortality and cause of death in inpatients with cerebral infarction. Methods The clinical data of 515 patients with cerebral infarction as the underlying cause of death from January 2005 to December 2009 were analyzed retrospectively. The hospital mortality, direct cause of death,and constituent ratio of the cause of death were calculated. The clinical features,such as classification of the Trial of Org 10 172 in acute stroke treatment( TOAST),age and duration of hospital-ization were analyzed. Results ( 1 )The hospital mortalities in patients with cerebral infarction from 2005 to 2009 were 2. 0%(91/4 659),2. 1%(110/5 264),1. 9%(95/5 035),1. 2%(100/8 656),and 1. 0%(119/11 640),respectively. The overall mortality rate was 1. 5%(515/35 254),basically had a declining trend year by year(χ2 =42. 39;P<0. 01).(2)The mortalities of the inpatients with cerebral infarction in the young( <45 years),middle-aged(45 to 59 years),elderly(60 to 74 years),and aged ( >74 years)groups were 1. 1%( 22/2 009 ),1. 0%( 112/11 158 ),1. 5%( 221/14 311 ),and 2. 1%(160/7 776),respectively. They increased with increasing age(P<0. 01).(3)The TOAST classification in 515 died patients were as follows:57. 3%(n=295)for large-artery atherosclerosis,19. 4%(n=100) for cardioembolism,14. 4%(n=74)for cryptogenic stroke,7. 0%(n=36)for small-artery occlusion and 1. 9%(n=10)for other reasons. The five leading direct cause of death were cerebral hernia 49. 3%(n=254),primary central respiratory and circulatory failure 25.0%(n=129),pneumonia 8. 9%(n =46), cerebral-cardiac syndrome 5. 8%( n =30 ),and multiple organ failure 5. 6%( n =29 ).( 4 ) The mean age of death was 67 ± 12 years old. The patients who died of cerebral hernia and primary central respiratory and circulatory failure were younger than those who died of pneumonia(65 ± 13,68 ± 11,and 75 ± 10,respectively;all P<0. 01). The median length of hospital stay was 3 days. The length of hospital stay in patients who died of hernia,primary central respiratory and circulatory failure,and cerebral-cardiac syndrome were significantly shorter than those who died of pneumonia and multiple organ failure( the median length of hospital stay was 3. 0,3. 0,3. 0,12. 5,and 9. 0 days,respectively;all P <0. 05). Conclusions The mortality of hospitalized patients with cerebral infarction have a declining trend year by year. Brain disease itself is the most important reason of early death for patients with cerebral infarction, indicating that it is the important point of prevention and treatment in clinical work.

Objective To study the therapeutic effects of Cordyceps polysaccharide (CP) on adenine-induced chronic renal failure(CRF)in rats. Methods CRF model was induced by Adenine ig .The rats were randomized into normal group, model group, CP high, moderate, Low-dosage groups and Dexamethasone group. The models of adenine-induced nephrosis were established by intragastric administration of adenine 300 mg/kg for 21 days. After treatment, renal function, biochemical indicators, kidney index, renal pathologic changes and serum TNF-? were observed. Results Compared with the model group, the degree injury of renal function in CP groups was palliated significant, renal pathologic changes were palliated significant, renal index and content of serum TNF-? were both decreased significant. Conclusion CP has a therapeutic and preventive effect on adenine-induced CRF, and can prevent the generation and development of CRF, improve renal function.

OBJECTIVE:To establish a method for the simultaneous determination of baicalin,baicalein and wogonin in Hua-tan pingchuan tablet. METHODS:HPLC was performed on the column was Diamonsil C18 with mobile phase of methanol-0.1%phosphoric acid(gradient elution)at a flow rate of 1.0 ml/min,detection wavelength was 277 nm,column temperature was 30 ℃, and the injection volume was 10 μl. RESULTS:The linear range was 0.069 04-0.690 4 μg for baicalin(r=0.999 4),0.054 56-0.5456 μg for baicalein(r=0.999 6)and 0.030 36-0.303 6 μg for wogonin(r=0.999 1);RSDs of precision,stability and reproduc-ibility tests were lower than 2%;recoveries were 97.64%-99.06%(RSD=0.57%,n=6),98.31%-100.64%(RSD=0.85%,n=6) and 97.53%-99.48%(RSD=0.76%,n=6). CONCLUSIONS:The method is simple,stable and reproducible,and can be used for the contents determination of baicalin,baicalein and wogonin in Huatan pingchuan tablet.

OBJECTIVE:To investigate the effect of Cyslosorus acuminatus flavonone glycoside (CAF) on kidney epitheli-al-mesenchymal transition(EMT)in rats with diabetic kidney disease(DKD). METHODS:Rats were randomly divided into nor-mal group(normal saline),model group(normal saline),positive group [rosiglitazone,0.4 mg/(kg·d)],CAF high-dose and low-dose groups [12.5,25 mg/(kg·d)],10 in each group. Except for normal group,other groups were intraperitoneally injected strepto-zotocin(60 mg/kg)+high fat diet to induce DKD,and intragastrically administrated related medicines in 13-16 weeks. After the ex-perimental period,fasting blood glucose level and serum creatinine(Scr),blood urea nitrogen(BUN)contents of rats were detect-ed,collagen deposition and basement membrane thickening in kidney tissue were observed. Immunohistochemistry was used to de-tect α-smooth muscle actin(α-SMA),fibronectin,epithelial cadherin(E-cadherin)expressions in kidney tissue,and Western blot was used to determine the glycogen synthase kinase 3β(GSK-3β),phosphorylated GSK-3β(p-GSK-3β),β-catenin expressions in kidney tissue. RESULTS:Compared with normal group,fasting blood glucose level,Scr and BUN contents in model group were significantly increased (P<0.01);kidney tissue showed obvious collagen deposition and basement membrane thickening;theα-SMA,fibronectin,β-catenin expression levels and GSK-3β phosphorylation degree in kidney tissue were significantly increased (P<0.01),while E-cadherin expression levels was significantly decreased(P<0.01). Compared with model group,fasting blood glucose level,Scr and BUN contents in each administration group were significantly reduced(P<0.05 or P<0.01);collagen depo-sition and basement membrane thickening in kidney tissue were significantly improved;the α-SMA,fibronectin,and β-catenin ex-pression levels and GSK-3β phosphorylation degree in kidney tissue were significantly decreased (P<0.05 or P<0.01),while E-cadherin expression levels in positive group and CAF high-dose group were significantly increased(P<0.01). CONCLUSIONS:CAF can inhibit the kidney EMT of rats with DKD,the molecular mechanism may be associated with downregulating β-catenin ex-pression and inhibiting GSK-3βphosphorylation inactivation.

A catalytic spectrophotometric method for the determination of micro amounts of osmium has been established based on the catalytic action of Os(Ⅳ) on the oxidation fading reaction of chlorophosphonazo-mA with KIO4 in alkaline-medium. The reaction conditions were optimized by orthogonal experimental design. The detection limit for osmium was 2.0 μg/L.Beer＇s law was obeyed in the range from 7.0 to 25.0 μg/L for Os(Ⅳ). The method has been applied to the determination of micro amounts of Os(Ⅳ) in concentrate of noble metals and secondary alloy,both of the relative errors were 0.9%. Recoveries varied from 95.38% to 106.0%.

Objective: To study the effect of Bazhen decoction on red blood cell immunity in rats with Qi deficiency.Methods:After the rats were forced to swim for two weeks continuously, the rat model of Qi deficiency was established. Bazhen group and normal group were fed with Bazhen decoction (20g?kg -1 ,daily), and distilled water for fourteen days, respectively. The changes in red blood cell c 3b receptor rosette rate (RBC.c 3bRR) and red blood cell immune complexes rosette rate (RBC.ICRR) were studied while the influences of Bazhen decoction on above mentioned parameters were observed. Results: In Qi deficiency syndrome the levels of RBC.c 3bRR were markedly depressed, while RBC.ICRR markedly elevated. After feeding Bazhen decoction orally to rats model with Qi deficiency syndrome, the levels of RBC. c 3bRR were elevated, while RBC.ICRR depressed (compared with Qi deficiency model group, P

Objective: To study the effect of XRK on mice's acute inflammation. Methods:The three XRL groups were fed on XRK of high, middle and low dosage, the positive group was fed on mezolin, and the control group was fed on distilled water. All groups were fed for three days, once per day. 30 minutes after the last treatment, Xylene (0.05 ml) was spreaded on mice's right ear in two sides, 15 minutes later, mice were put to death and its two ears were cut in same area, then weighed, calculated the swelling degree of its ears. Results: ① The swelling degrees in the three XRL groups were all lower significantly than that in the control group ( P

Objective To investigate and analyze the monitoring status of birth defects of perinatal infants in Hakka of Guangxi Zhuang Autonomous Region,and to provide evidence for reducing the incidence of birth defects and improving prevention decision for the quality of birth.Methods The data of 51 528 cases of perinatal birth defects monitoring were analyzed in Bobai and Luchuan counties in 2015.Results The distribution of birth defects in the perinatal infants of Hakka was more than 75.14%,28.8% of the birth defects occurred in 28 weeks,51 528 cases of perinatal birth in hospital,birth defects of ≥28 weeks in 384 cases.The incidence rate of birth defects was 28.5%, the rate of birth was 7.45‰.The birth defect of ≥28 weeks was diagnosed,35 cases were fetal edema syndrome, accounted for 9.11%.34 cases were congenital heart disease,accounted for 8.85%,30 cases were cleft lip with cleft palate,accounted for 7.81%.Congenital hydrocephalus in 5 cases,accounted for 1.30%;other in 251 cases,accoun-ted for 65.35%.The diagnosed time distribution of birth defects of ≥28 weeks:prenatal diagnosis accounted for 21.18%,postnatal 7 days accounted for 78.82%.The outcome of ≥28 weeks of perinatal birth defects in Hakka:live birth accounted for 73.18%,fetal death accounted for 20.57%,stillbirth accounted for 1.30%,seven days of death accounted for 4.94%.Conclusion The perinatal birth defects in Hakka is live births to the main,the prevention of perinatal birth defects in children live birth measures should be strengthened,the detection of birth defects should be strengthened and the pregnancy of artificial birth defects should be terminated,so as to improve the quality of the birth population.

Objective To explore any protective effect of hyperbaric oxygen in traumatic brain injury and its effect on the expression of silent information regulator 1 ( SIRT1) . Methods Sixty mice were randomly divided into a control group (n=20), a brain injury group (TBI, n=20) and a hyperbaric oxygen therapy group (TBI+HBO, n=20) . The mice in the TBI and TBI + HBO groups were given massive blows to establish closed brain injuries, while in the control group the scalp was incised and a bone window was removed without brain damage. The mice in the TBI + HBO group were given hyperbaric oxygen treatment twice per day for five days, while those in the TBI and control groups were put in the hyperbaric chamber but not given HBO treatment. At one hour after the trauma and on 5 days afterward, the neurological functioning of the mice was measured to generate neurological severity scores. Brain tissue was resected for triphenyl tetrazolium staining to measure the infarct area. Cortical neurons were isolated to eval-uate the SIRT1 expression using immunofluorescence and Western blotting. Results No significant difference in the average NSS score was observed between the TBI and TBI+HBO groups one hour after modeling. The average NSS score in the TBI group subsequently increased and then decreased gradually until the fifth day. The average NSS score of the TBI+HBO group was significantly lower than that of the TBI group after the onset of the treatment at the differ-ent time points, decreasing to (2.11±0.43) on the 5thday compared with (4.06±0.54) in the TBI+HBO group. On the 2nd day after the trauma, the cerebral infarction areas of the TBI and TBI+HBO groups were significantly larger than in the control group. During the treatment, the infarction area of the TBI+HBO group decreased gradually until on the 5th day it was significantly smaller than that of the TBI group. Traumatic brain injury significantly down-regula-ted SIRT1 protein compared with the control group, but the hyperbaric oxygen therapy significantly increased the ex-pression of SIRT1 compared with the TBI group. Conclusion Hyperbaric oxygen therapy can significantly relieve traumatic brain injury, reducing NSS scores and the infarcted area and enhancing SIRT1 expression, at least in mice.